Traditional remedies have ranged from warm baths (if the pain lasts long enough to draw a bath), warm to hot enemas, relaxation techniques, and various medications.

Yoga pose "downward facing dog" -Adho Mukha Svanasana, or modification from it seems to help to relax the muscles and ease the pain. The idea of the yoga pose is that the position will force the muscles to relax and therefore tension will relieve over time. Also relaxing one's jaw muscles will help to relax the muscles in rectal area, method used by women giving birth.

In patients who suffer frequent, severe, prolonged attacks, inhaled salbutamol has been shown in some studies to reduce their duration.

The use of botulinum toxin has been proposed as analgesic, and low dose diazepam at bedtime has been suggested as preventative.

The most common approach for mild cases is simply reassurance and topical treatment with calcium-channel blocker (diltiazem, nifedipine) ointment, salbutamol inhalation and sublingual nitroglycerine.For persistent cases, local anesthetic blocks, clonidine or Botox injections can be considered. Supportive treatments directed at aggravating factors include high-fiber diet, withdrawal of drugs which have gut effects (e.g., drugs that provoke or worsen constipation including narcotics and oral calcium channel blockers; drugs that provoke or worsen diarrhea including quinidine, theophylline, and antibiotics), warm baths, rectal massage, perineal strengthening exercises, anti-cholinergic agents, non-narcotic analgesics, sedatives or muscle relaxants such as diazepam.

High-voltage pulsed galvanic stimulation (HGVS) has been shown to be of prophylactic benefit, to reduce the incidence of attacks. The patient is usually placed in the left lateral decubitus position and a sterile probe is inserted into the anus. The negative electrode is used and the stimulator is set with a pulse frequency of 80 to 120 cycles per second. The voltage (intensity) is started at 0, progressively raised to a threshold of patient discomfort, and then is decreased to a level that the patient finds comfortable. As the patient's tolerance increases, the voltage can be gradually increased to 250 to 350 Volts. Each treatment session usually lasts between 15 and 60 minutes. Several studies have reported short-term success rates that ranged from 65 to 91%.

An anorectal abscess is an infection that forms a pocket of pus within the tissues around the anus. It is treated surgically by incision and drainage.

Bacterial, viral, and protozoal infections may occur in the area surround the rectum. These may be the result of a sexually transmitted disease.

There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. Heightened mast cell activation has been proposed to be a common factor among FGIDs, contributing to visceral hypersensitivity as well as epithelial, neuromuscular, and motility dysfunction.

If the diagnostic workup reveals a systemic disease process, directed therapies to treat that underlying cause should be initiated. If the amaurosis fugax is caused by an atherosclerotic lesion, aspirin is indicated, and a carotid endarterectomy considered based on the location and grade of the stenosis. Generally, if the carotid artery is still patent, the greater the stenosis, the greater the indication for endarterectomy. "Amaurosis fugax appears to be a particularly favorable indication for carotid endarterectomy. Left untreated, this event carries a high risk of stroke; after carotid endarterectomy, which has a low operative risk, there is a very low postoperative stroke rate." However, the rate of subsequent stroke after amaurosis is significantly less than after a hemispheric TIA, therefore there remains debate as to the precise indications for which a carotid endarterectomy should be performed. If the full diagnostic workup is completely normal, patient observation is recommended.

Functional gastrointestinal disorders are very common. Globally, irritable bowel syndrome and functional dyspepsia alone may affect 16–26% of the population.

As of 2017, eleven disease-modifying medications have been approved by regulatory agencies for relapsing-remitting multiple sclerosis (RRMS). They are interferon beta-1a, interferon beta-1b, glatiramer acetate, mitoxantrone, natalizumab, fingolimod, teriflunomide, dimethyl fumarate, alemtuzumab, daclizumab, and ocrelizumab.

Their cost effectiveness as of 2012 is unclear. In May 2016 the FDA approved daclizumab for the treatment of relapsing multiple sclerosis in adults, with requirements for postmarketing studies and submission of a formal risk evaluation and mitigation strategy. In March 2017 the FDA approved ocrelizumab, a humanized anti-CD20 monoclonal antibody, as a treatment for RRMS, with requirements for several Phase IV clinical trials.

In RRMS they are modestly effective at decreasing the number of attacks. The interferons and glatiramer acetate are first-line treatments and are roughly equivalent, reducing relapses by approximately 30%. Early-initiated long-term therapy is safe and improves outcomes. Natalizumab reduces the relapse rate more than first-line agents; however, due to issues of adverse effects is a second-line agent reserved for those who do not respond to other treatments or with severe disease. Mitoxantrone, whose use is limited by severe adverse effects, is a third-line option for those who do not respond to other medications. Treatment of clinically isolated syndrome (CIS) with interferons decreases the chance of progressing to clinical MS. Efficacy of interferons and glatiramer acetate in children has been estimated to be roughly equivalent to that of adults. The role of some newer agents such as fingolimod, teriflunomide, and dimethyl fumarate, as of 2011, is not yet entirely clear.

As of 2017, rituximab was widely used off-label to treat RRMS.

As of 2017, rituximab has been widely used off-label to treat progressive primary MS. In March 2017 the FDA approved ocrelizumab, as a treatment for primary progressive MS, the first drug to gain that approval, with requirements for several Phase IV clinical trials.

, only one medication, mitoxantrone, has been approved for secondary progressive MS. In this population tentative evidence supports mitoxantrone moderately slowing the progression of the disease and decreasing rates of relapses over two years.

Quick determination of the cause may lead to urgent measures to save the eye and life of the patient. High clinical suspicion should be kept for painless vision loss in patients with atherosclerosis, deep venous thrombosis, atrial fibrillation, pulmonary thromboembolism or other previous embolic episodes. Those caused by a carotid artery embolism or occlusion have the potential for further stroke by detachment of embolus and migration to an end-artery of the brain. Hence, proper steps to prevent such an eventuality need to be taken.

Retinal arterial occlusion is an ophthalmic emergency, and prompt treatment is essential. Completely anoxic retina in animal models causes irreversible damage in about 90 minutes. Nonspecific methods to increase blood flow and dislodge emboli include digital massage, 500 mg IV acetazolamide and 100 mg IV methylprednisolone (for possible arteritis). Additional measures include paracentesis of aqueous humor to decrease IOP acutely. An ESR should be drawn to detect possible giant cell arteritis. Improvement can be determined by visual acuity, visual field testing, and by ophthalmoscopic examination.

At a later stage, pan-retinal photocoagulation (PRP) with an argon laser appears effective in reducing the neovascular components and their sequelae.

The visual prognosis for ocular ischemic syndrome varies from usually poor to fair, depending on speed and effectiveness of the intervention. However, prompt diagnosis is crucial as the condition may be a presenting sign of serious cerebrovascular and ischemic heart diseases.

In 2009, the Undersea and Hyperbaric Medical Society added "central retinal artery occlusion" to their list of approved indications for hyperbaric oxygen (HBO). When used as an adjunctive therapy, the edema reducing properties of HBO, along with down regulation of inflammatory cytokines may contribute to the improvement in vision. Prevention of vision loss requires that certain conditions be met: the treatment be started before irreversible damage has occurred (over 24 hours), the occlusion must not also occur at the ophthalmic artery, and treatment must continue until the inner layers of the retina are again oxygenated by the retinal arteries.

The experience of amaurosis fugax is classically described as a temporary loss of vision in one or both eyes that appears as a black "curtain coming down vertically into the field of vision in one eye;" however, this altitudinal visual loss is relatively uncommon. In one study, only 23.8 percent of patients with transient monocular vision loss experienced the classic "curtain" or "shade" descending over their vision. Other descriptions of this experience include a monocular blindness, dimming, fogging, or blurring. Total or sectorial vision loss typically lasts only a few seconds, but may last minutes or even hours. Duration depends on the cause of the vision loss. Obscured vision due to papilledema may last only seconds, while a severely atherosclerotic carotid artery may be associated with a duration of one to ten minutes. Certainly, additional symptoms may be present with the amaurosis fugax, and those findings will depend on the cause of the transient monocular vision loss.

Those experiencing amaurosis are usually advised to consult a physician immediately as any form of vision loss, even if temporary, is a symptom that may indicate the presence of a serious ocular or systemic problem.

An antiplatelet, such as aspirin, is started for secondary prevention of stroke after most TIAs. An exception is TIAs due to blood clots originating from the heart, in which case anticoagulants are generally recommended. After TIA or minor stroke, aspirin therapy has been shown to reduce the short-term risk of recurrent stroke by 60-70%, and the long-term risk of stroke by 13%.

The typical therapy may include aspirin alone, a combination of aspirin plus extended-release dipyridamole, or clopidogrel alone. Clopidogrel and aspirin have similar efficacies and side effect profiles. Clopidogrel is more expensive and has a slightly decreased risk of GI bleed. There is some evidence that giving both aspirin and clopidogrel within 24 hours of a TIA or minor stroke is more effective than aspirin alone. Another antiplatelet, ticlopidine, is rarely used due to increased side effects.

Leber's congenital amaurosis is an inherited disease resulting in optic atrophy and secondary severe vision loss or blindness. It was first described by Theodore Leber in the 19th century.

Amaurosis fugax (Latin: "fugax" meaning "fleeting") is a temporary loss of vision in one eye caused by decreased blood flow (ischemia) to the retina. It may also be caused by embolization from atherosclerotic plaques in the ipsilateral (same side) internal carotid artery. It is a type of transient ischaemic attack (TIA). Those experiencing amaurosis usually experience complete symptom resolution within a few minutes. In a small minority of those who experience amaurosis, stroke or permanent vision loss results. Diabetes, hypertension and smoking are factors known to increase the risks of suffering this condition. It also can be the result of surgical repair to the mitral valve, when very small emboli may break away from the site of the repair, while the patient's tissue grows to cover the plastic annuloplasty band.

Quinidine toxicity can lead to cinchonism and also to quinine amaurosis.

Anticoagulants may be started if the TIA is thought to be attributable to atrial fibrillation. Atrial fibrillation is an abnormal heart rhythm that may cause the formation of blood clots that can travel to the brain, resulting in TIAs or ischemic strokes. Atrial fibrillation increases stroke risk by five times, is thought to cause 10-12% of all ischemic strokes in the US. Anticoagulant therapy can decrease the relative risk of ischemic stroke in those with atrial fibrillation by 67% Warfarin is a common anticoagulant used, but direct acting oral anticoagulants (DOACs), such as apixaban, have been shown to be equally effective while also conferring a lower risk of bleeding. Generally, anticoagulants and antiplatelets are not used in combination, as they result in increased bleeding risk without a decrease in stroke risk. However, combined antiplatelet and anticoagulant therapy may be warranted if the patient has symptomatic coronary artery disease in addition to atrial fibrillation.

Sometimes, myocardial infarction (“heart attack”) may lead to the formation of a blood clot in one of the chambers of the heart. If this is thought to be the cause of the TIA, people may be temporarily treated with warfarin or other anticoagulant to decrease the risk of future stroke.

Treatment of an episode of cholesterol emboli is generally symptomatic, i.e. it deals with the symptoms and complications but cannot reverse the phenomenon itself. In kidney failure resulting from cholesterol crystal emboli, statins (medication that reduces cholesterol levels) have been shown to halve the risk of requiring hemodialysis.

Options include:

- Medications alone (an antiplatelet drug (or drugs) and control of risk factors for atherosclerosis).

- Medical management plus carotid endarterectomy or carotid stenting, which is preferred in patients at high surgical risk and in younger patients.

- Control of smoking, high blood pressure, and high levels of lipids in the blood.

The goal of treatment is to reduce the risk of stroke (cerebrovascular accident). Intervention (carotid endarterectomy or carotid stenting) can cause stroke; however, where the risk of stroke from medical management alone is high, intervention may be beneficial. In selected trial participants with asymptomatic severe carotid artery stenosis, carotid endarterectomy reduces the risk of stroke in the next 5 years by 50%, though this represents a reduction in absolute incidence of all strokes or perioperative death of approximately 6%. In most centres, carotid endarterectomy is associated with a 30-day stroke or mortality rate of < 3%; some areas have higher rates.

Clinical guidelines (such as those of National Institute for Clinical Excellence (NICE) ) recommend that all patients with carotid stenosis be given medication, usually blood pressure lowering medications, anti-clotting medications, anti-platelet medications (such as aspirin or clopidogrel), and especially statins (which were originally prescribed for their cholesterol-lowering effects but were also found to reduce inflammation and stabilize plaque).

NICE and other guidelines also recommend that patients with "symptomatic" carotid stenosis be given carotid endarterectomy urgently, since the greatest risk of stroke is within days. Carotid endarterectomy reduces the risk of stroke or death from carotid emboli by about half.

For people with stenosis but no symptoms, the interventional recommendations are less clear. Such patients have a historical risk of stroke of about 1-2% per year. Carotid endarterectomy has a surgical risk of stroke or death of about 2-4% in most institutions. In the large Asymptomatic Carotid Surgery Trial (ACST) endarterectomy reduced major stroke and death by about half, even after surgical death and stroke was taken into account. According to the Cochrane Collaboration the absolute benefit of surgery is small. For intervention using stents, there is insufficient evidence to support stenting rather than open surgery, and several trials, including the ACST-2, are comparing these 2 procedures.

Ocular ischemic syndrome is the constellation of ocular signs and symptoms secondary to severe, chronic arterial hypoperfusion to the eye. Amaurosis fugax is a form of acute vision loss caused by reduced blood flow to the eye; it may be a warning sign of an impending stroke, as both stroke and retinal artery occlusion can be caused by thromboembolism due to atherosclerosis elsewhere in the body (such as coronary artery disease and especially carotid atherosclerosis). Consequently, those with transient blurring of vision are advised to urgently seek medical attention for a thorough evaluation of the carotid artery. Anterior segment ischemic syndrome is a similar ischemic condition of anterior segment usually seen in post-surgical cases. Retinal artery occlusion (such as central retinal artery occlusion or branch retinal artery occlusion) leads to rapid death of retinal cells, thereby resulting in severe loss of vision.

The largest clinical trial performed, CREST, randomized patients at risk for a stroke from carotid artery blockage to either open surgery (carotid endarterectomy) or carotid stent placement with embolic protection. This trial followed patients for 4 years and found no overall difference in the primary end point of both treatment arms (myocardial infarctions, any perioperative strokes or ipsilateral strokes within 4 years, or death during procedure). Patients assigned to the surgical arm experienced more perioperative myocardial infarctions compared to the stenting group; however, the difference was not statistically significant (6.8% vs or 7.2% HR for stenting is 1.1 CI 0.81-1.51 P value 0.51) whereas patients assigned to the carotid stent arm experienced more periprocedural strokes compared to endarteretomy (6.4% vs 4.7% HR for stenting 1.5 P-0.03). There was no mortality difference and no difference for major (disabling) strokes between surgery and stenting. It was noted that there did seem to exist an age cutoff where below 75 years old endarterectomy provided more positive outcomes and over 75 stenting offered a better risk profile. However, it should be noted that the CREST trial was not designed for subgroup analysis and thus not powered enough to draw any statistically significant conclusions. A later study published in 2013 evaluated how these perioperative complications affect long-term survival. This study showed that experiencing a stroke within the first year conferred a two-fold lower survival rate (Hazard Ratio(HR) 6.6 [CI 3.7-12]) than those who experienced a perioperative myocardial infarction at two years post intervention (HR 3.6 [CI 2-6.8]). This difference in mortality, however, converges and becomes negligible at 5 years (HR 2.7 [CI 1.7-4.3] vs HR 2.8 [CI 1.8-4.3]). A 2010 study found benefits (reduced strokes) from carotid endarterectomy in those without symptoms who are under 75.

The four goals of the treatment of eclampsia are to stop and prevent further convulsions, to control the elevated blood pressure, to deliver the baby as promptly as possible, and to monitor closely for the onset of multi-organ failure.

The agents of choice for blood pressure control during eclampsia are hydralazine and/or labetalol. This is because of their effectiveness, lack of negative effects on the fetus, and mechanism of action.

The symptoms experienced in cholesterol embolism depend largely on the organ involved. Non-specific symptoms often described are fever, muscle ache and weight loss. Embolism to the legs causes a mottled appearance and purple discoloration of the toes, small infarcts and areas of gangrene due to tissue death that usually appear black, and areas of the skin that assume a marbled pattern known as "livedo reticularis". The pain is usually severe and requires opiates. If the ulcerated plaque is below the renal arteries the manifestations appear in both lower extremities. Very rarely the ulcerated plaque is below the aortic bifurcation and those cases the changes occur only in one lower extremity.

Kidney involvement leads to the symptoms of renal failure, which are non-specific but usually cause nausea, reduced appetite (anorexia), raised blood pressure (hypertension), and occasionally the various symptoms of electrolyte disturbance such as an irregular heartbeat. Some patients report hematuria (bloody urine) but this may only be detectable on microscopic examination of the urine. Increased amounts of protein in the urine may cause edema (swelling) of the skin (a combination of symptoms known as nephrotic syndrome).

If emboli have spread to the digestive tract, reduced appetite, nausea and vomiting may occur, as well as nonspecific abdominal pain, gastrointestinal hemorrhage (vomiting blood, or admixture of blood in the stool), and occasionally acute pancreatitis (inflammation of the pancreas).

Both the central nervous system (brain and spinal cord) and the peripheral nervous system may be involved. Emboli to the brain may cause stroke-like episodes, headache and episodes of loss of vision in one eye (known as amaurosis fugax). Emboli to the eye can be seen by ophthalmoscopy and are known as plaques of Hollenhorst. Emboli to the spinal cord may cause paraparesis (decreased power in the legs) or cauda equina syndrome, a group of symptoms due to loss of function of the distal part of the spinal cord - loss of control over the bladder, rectum and skin sensation around the anus. If the blood supply to a single nerve is interrupted by an embolus, the result is loss of function in the muscles supplied by that nerve; this phenomenon is called a "mononeuropathy".